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Related Concept Videos

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Related Experiment Video

Updated: Jan 20, 2026

Studying Age-dependent Genomic Instability using the S. cerevisiae Chronological Lifespan Model
08:46

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Nuclear pore links Fob1-dependent rDNA damage relocation to lifespan control.

Yamato Okada1, Mina Iwaki1, Kyosuke Hagiri1

  • 1Laboratory of Molecular Biochemistry, Graduate School of Agricultural Science, Tohoku University, Sendai, Miyagi, Japan.

FEBS Open Bio
|January 19, 2026
PubMed
Summary
This summary is machine-generated.

In budding yeast, damaged ribosomal DNA (rDNA) moves to the nuclear periphery, interacting with nuclear pores. This spatial organization by nuclear pores is crucial for maintaining genome stability and cell longevity.

Keywords:
Fob1Saccharomyces cerevisiaegenome stabilitylifespannuclear poreribosomal RNA gene (rDNA)

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Area of Science:

  • Cell Biology
  • Genetics
  • Molecular Biology

Background:

  • Replication fork blocking protein Fob1 in budding yeast causes DNA double-strand breaks at the ribosomal RNA gene (rDNA) locus.
  • rDNA damage is linked to genomic instability, reduced replicative lifespan, and spatial relocation of breaks from the nucleolus to the nuclear periphery.
  • The precise organization and functional significance of these spatial transitions in genome stability and aging remain poorly understood.

Purpose of the Study:

  • To investigate the subnuclear localization of site-specific rDNA breaks.
  • To elucidate the functional relationship between damaged rDNA and nuclear pores.
  • To understand how spatial organization of rDNA damage influences genome stability and replicative lifespan.

Main Methods:

  • Quantitative fluorescence microscopy was employed to analyze the subnuclear localization of damaged rDNA.
  • Site-specific rDNA breaks were induced and tracked within budding yeast cells.
  • Genetic manipulations, including deletion of Fob1 and disruption of nuclear pore association, were performed.

Main Results:

  • Damaged rDNA was observed to accumulate at the nucleolar-nucleoplasmic interface, adjacent to the nuclear envelope.
  • Cells lacking nuclear pore association exhibited significant rDNA instability, partially rescued by Fob1 deletion.
  • Disruption of nuclear pore association shortened replicative lifespan, with partial rescue by Fob1 deletion, indicating both Fob1-dependent and independent pathways.

Conclusions:

  • Nuclear pores play a role in spatially organizing Fob1-induced rDNA damage at the nuclear periphery.
  • This spatial organization is critical for maintaining rDNA stability and extending replicative lifespan in budding yeast.
  • Nuclear pores contribute to longevity through both Fob1-dependent and Fob1-independent mechanisms related to rDNA damage.